Involvement of p38 MAP kinase and Smad3 in TGF-β-mediated mast cell functions

Masayuki Funaba, Teruo Ikeda, Masaru Murakami, Kenji Ogawa, Yoshii Nishino, Kunihiro Tsuchida, Hiromu Sugino, Matanobu Abe

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11 Citations (Scopus)


Transforming growth factor-β (TGF-β) modulates functions of bone marrow-derived cultured mast cells (BMMCs); cell maturation (up-regulation of mouse mast cell proteases (mmcps)), growth arrest and migration. We investigated the roles of p38 MAP kinase and Smad3 in TGF-β-mediated cell responses in BMMCs. Treating BMMCs with TGF-β induced the phosphorylation of p38 within 2 h and persisted for 24 h. The involvement of p38 in TGF-β-induced cell responses depended upon mast cell functions; it was necessary for up-regulation of mmcp-1 and migration, but not for up-regulation of mmcp-7 and inhibition of metabolic activity. New protein synthesis was required for the up-regulation of mmcp-1 but not mmcp-7 in response to TGF-β treatment, and stabilization of mRNA was partially responsible for the increase in gene transcript of mmcp-1. The decrease in metabolic activity in response to TGF-β treatment was smaller in Smad3-deficient BMMCs compared to wild-type BMMCs. Maximal migration was detected at a TGF-β concentration of 40 fM in wild-type BMMCs, whereas TGF-β-induced migration was absent in Smad3-deficient BMMCs. Thus, the roles of p38 and Smad3 are different among TGF-β-mediated cell responses in BMMCs.

Original languageEnglish
Pages (from-to)2154-2161
Number of pages8
JournalCellular Signalling
Issue number12
Publication statusPublished - 12-2006
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Cell Biology


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